ArticleThe Journal of physiology2012
Rapid reversal of impaired inhibitory and excitatory transmission but not spine dysgenesis in a mouse model of mental retardation.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Architects of the Developing Brain: Cytoskeleton-Organizing Molecules in Neurodevelopmental Disorders.Cells · 2026Review
- Keeping Excitation-Inhibition Ratio in Balance.International journal of molecular sciences · 2022Review
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- Neuronal Cytoskeleton in Intellectual Disability: From Systems Biology and Modeling to Therapeutic Opportunities.International journal of molecular sciences · 2021Review
- Article
- Review
- GRAF2, WDR44, and MICAL1 mediate Rab8/10/11-dependent export of E-cadherin, MMP14, and CFTR ΔF508.The Journal of cell biology · 2020Article
- ROCK/PKA Inhibition Rescues Hippocampal Hyperexcitability and GABAergic Neuron Alterations in a Oligophrenin-1 Knock-Out Mouse Model of X-Linked Intellectual Disability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Article
- Prion acute synaptotoxicity is largely driven by protease-resistant PrPSc species.PLoS pathogens · 2018Article
- Rho GTPases in Intellectual Disability: From Genetics to Therapeutic Opportunities.International journal of molecular sciences · 2018Review
- Activation of RHO-1 in cholinergic motor neurons competes with dopamine signalling to control locomotion.PloS one · 2018Article
- Protein Kinase A Deregulation in the Medial Prefrontal Cortex Impairs Working Memory in Murine Oligophrenin-1 Deficiency.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Pharmacological rescue of adult hippocampal neurogenesis in a mouse model of X-linked intellectual disability.Neurobiology of disease · 2017Article
- Rho Kinase Inhibition Is Essential During In Vitro Neurogenesis and Promotes Phenotypic Rescue of Human Induced Pluripotent Stem Cell-Derived Neurons With Oligophrenin-1 Loss of Function.Stem cells translational medicine · 2016Article
- Impaired Dendritic Development and Memory in Sorbs2 Knock-Out Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Oligophrenin-1 Connects Exocytotic Fusion to Compensatory Endocytosis in Neuroendocrine Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Lack of the presynaptic RhoGAP protein oligophrenin1 leads to cognitive disabilities through dysregulation of the cAMP/PKA signalling pathway.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Article
- Reduced gamma oscillations in a mouse model of intellectual disability: a role for impaired repetitive neurotransmission?PloS one · 2014Article
- Developmental vulnerability of synapses and circuits associated with neuropsychiatric disorders.Journal of neurochemistry · 2013Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Intellectual disability affects 2-3% of the population: those due to mutations of the X-chromosome are a major cause of moderate to severe cases (1.8/1000 males). Established theories ascribe the cellular aetiology of intellectual disability to malformations of dendritic spines. Recent work has identified changes in synaptic physiology in some experimental models. Here, we investigated the pathophysiology of a mouse model of intellectual disability using electrophysiological recordings combined with confocal imaging of dentate gyrus granule neurons. Lack of oligophrenin-1 resulted in reductions in dendritic tree complexity and mature dendritic spine density and in evoked and spontaneous EPSCs and IPSCs. In the case of inhibitory transmission, the physiological change was associated with a reduction in the readily releasable pool and vesicle recycling which impaired the efficiency of inhibitory synaptic transmission. Acute inhibition of the downstream signalling pathway of oligophrenin-1 fully reversed the functional changes in synaptic transmission but not the dendritic abnormalities. The impaired inhibitory (as well as excitatory) synaptic transmission at frequencies associated with cognitive function suggests a cellular mechanism for the intellectual disability, because cortical oscillations associated with cognition normally depend on inhibitory neurons firing on every cycle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.